The elucidation of the molecule mechanism of the drug susceptibility in the chemotherapy for the oligodendroglioma
The elucidation of the molecule mechanism of the drug susceptibility in the chemotherapy for the oligodendroglioma
批准号:
13470284
负责人:
TANAKA Minoru
金额:
$8.77万
依托单位:
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (B)
财政年份:
2001
资助国家:
日本
项目状态:
已结题
起止时间:
2001 至 2004
中文摘要
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英文摘要
This research investigated deficit of a chromosome (1p, 19q, 10q, CDKN2N), and variation of a gene TP53, and amplification of EGFR or CDK4 in many clinical samples of a tumor bank. Many of tumors accompanied by 1p deficit are oligodendroglioma, and it is in about 60% of the oligodendroglioma. It was simultaneously accompanied by the deficit of 19q. In the oligodendroglioma without the deficit of chromosome 1p, many gene variation of p53 was accepted.Next, the drug susceptibility in chemotherapy related gene of the oligodendroglioma. A profile analysis of chromosome 1p was performed by a microarray (DNA chip) for the purpose of the antioncogene identification assumed to be on chromosome 1p. Consequently, chemotherapy susceptibility is high among oligodendroglioma accompanied by the deficit of single-sided allele of 1p. For the first time 209 genes changing intentionally on chromosome 1p, and the 123 genes considered an antioncogene, were identified.Furthermore, for astrocytoma or glioblastoma gene expression profile analysis was performed by Gene chip, and comparison analysis with the oligodendroglioma was enforced. It became clear that the gene amplified in oligodendroglioma with high chemotherapy susceptibility was the gene cluster to a neuron. Moreover, some genes discovered characteristic of astrocytoma or the glioblastoma were also identified. Although, as for two examples of astrocytoma (WHO Grade II), the discovery profile resembled glioblastoma (WHO Grade IV), the prognosis of these cases was actually poor and, also clinically, showed progress like glioblastoma.Thus, a gene expression profile can serve as a tool which presumes the prognosis of each case.
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Mukasa A, Ueki K, Matsumoto S, Tsutsumi S, Nishikawa R, Fujimaki T, Asai A, Kirino T, Aburatani H: "Distinction in gene expression profiles of oligodendrogliomas with and without allelic loss of 1p"Oncogene. (in press).
Mukasa A、Ueki K、Matsumoto S、Tsutsumi S、Nishikawa R、Fujimaki T、Asai A、Kirino T、Aburatani H:“具有和不具有 1p 等位基因丢失的少突胶质细胞瘤基因表达谱的区别”癌基因。
DOI:
--
发表时间:
期刊:
影响因子:
--
作者:
[]
通讯作者:
DOI:
10.1111/j.1750-3639.2004.tb00495.x
发表时间:
2004-01-01
期刊:
BRAIN PATHOLOGY
影响因子:
6.4
作者:
[Mukasa, A, Ueki, K, Aburatani, H]
通讯作者:
Aburatani, H
Correlation of histology and molecular genetic analysis of 1p,19q,10q,TP53,EGFR,CDK4,and CDKN2A in 91 astrocytic and oligodendroglial tumors.
91例星形细胞和少突胶质细胞肿瘤中1p、19q、10q、TP53、EGFR、CDK4和CDKN2A的组织学和分子遗传学分析的相关性。
DOI:
--
发表时间:
2002
期刊:
Clin Cancer Res. 8(1)
影响因子:
--
作者:
[Ueki K, Nishikawa R, Nakazato Y, Hirose T, Hirato J, Funada N, Fujimaki T, Hojo S, Kubo O, Ide T, Usui M, Ochiai C, Ito S, Takahashi H, Mukasa A, Asai A, Kirino T.]
通讯作者:
Kirino T.
DOI:
10.1038/sj.onc.1205495
发表时间:
2002-06-06
期刊:
ONCOGENE
影响因子:
8
作者:
[Mukasa, A, Ueki, K, Aburatani, H]
通讯作者:
Aburatani, H
Mukasa A, Ueki K, Matsumoto S, Tsutsumi S, Nishikawa R, Fujimaki T, Asai: "Distinction in gene expression profiles of oligodendrogliomas with and without allelic loss of 1p"Oncogene. 21(25). 3961-3968 (2002)
Mukasa A、Ueki K、Matsumoto S、Tsutsumi S、Nishikawa R、Fujimaki T、Asai:“具有和不具有 1p 等位基因丢失的少突胶质细胞瘤基因表达谱的区别”癌基因。
DOI:
--
发表时间:
期刊:
影响因子:
--
作者:
[]
通讯作者:
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Investigation for Common Molecular Mechanisms by Comparison of EST from Purified Germ Cells
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Mechanism of prolactin action on induction of development, enlargement and inflammation of prostate -study with prolactin knockout mice-
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High density mapping of BAC end sequences onto medaka linkage groups
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Study of Extension of Functions of Iconic Workspace
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Studies on the Development of Selectively Modified Cyclodextrin Stationary Phases for HPLC
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